Developmental Pattern of Estrogen Receptor Expression in Female Mouse Genital Tracts

Abstract

The distribution of the estrogen receptor (ER) was investigated in neonatal female genital tracts (uterus, oviduct, cervix, and vagina) from days 1-22 after birth, using immunohistochemistry employing an anti-ER monoclonal antibody. In uteri, the ER in epithelial cells began to be observed by day 4. The number of positive epithelial cells and the staining intensity gradually increased until day 22 of age. On the other hand, uterine stroma cells gave a strong ER immunostaining even on day 1. The staining intensity reached a maximum by days 4-7 and then slightly decreased with age. In the oviduct, cervix, and vagina, epithelial cells showed positive ER immunostaining on day 1, and the intensity increased gradually until day 22. ER immunostaining in stroma cells was almost constant during the development period. The ER in both epithelial and stroma cells from these younger animals showed similar biochemical properties, i.e. an increased affinity for nuclei and resistance to extraction with PBS. Thus, during neonatal development of the female reproductive tract, ER is present not only in stroma cells but also in epithelial cells. This ER protein exhibits properties and characteristics similar to those of adult mice. The presence of ER suggests that some of the estrogen actions of cell proliferation, differentiation, and tissue abnormalities resulting from prenatal and postnatal estrogen administration may be mediated by receptor interactions.

Developmental changes of the oestrogen receptor-alpha and -beta mRNAs in the female reproductive organ of the rat--an analysis by in situ hybridization

“…Since the ER mRNA probe used in this study was picked from the A/B domain, it was expected to detect both ER 1 and 2 isoforms, which chiefly differ in the ligand domain (Patersson et al 1998). The present data was consistent with the results of several earlier studies which studied ER distribution by immunohistochemistry using perinatal tissues of mice (Yamashita et al 1989, Greco et al 1991, Jefferson et al 2000 and rats (Sar & Welsch 1999), binding assay using postnatal rats (Clark & Gorski 1972) and in situ hybridization for ER using postnatal rats (Fishman et al 1996). There are, however, a few discrepancies between our findings and some immunohistochemical reports.…”

Ontogeny of Estrogen Receptor (ER) .ALPHA. and .BETA. in the Female Reproductive Tissues of Mice Neonatally Exposed to Diethylstilbestrol.

“…The ontogeny of ERa in the female genital tract of vehicle-treated control mice was basically the same as the previous results examined with H-222 monoclonal antibody in untreated normal mice [37,39]. The present study demonstrated that DES-treatment up-regulates the expression of ERa in the epithelial cells in the oviducts, uteri, cervices and vaginae, and down-regulates the expression in the stromal cells at least until 10 days of age.…”

“…or normal rabbit IgG were used as the primary antibodies. Some sections were incubated with anti-ER rat monoclonal antibody (Abbott Laboratories, Abbot Park, IL) to compare with the previous our results concerning ontogenic ERa expression which were obtained from mice without any treatment [37]. After washing with PBS, they were then treated with anti-rabbit Ig, horseradish peroxidase (HRP) linked F(ab') 2 fragments or rat Ig, HRP linked F(ab') 2 fragments (Amersham Life Sci., UK), each 100-fold diluted with the blocking solution, for 90 min at room temperature.…”

“…The responses to exogenous estrogens were thought to be mediated through the ER system in the stroma, since earlier studies using steroid autoradiograph localized ERs only in the stromal cells but not in the epithelium in the female reproductive tract of neonatal mice [2]. However, immunohistochemical studies have demonstrated that ERa is present in the epithelium of the oviduct, cervix and vagina even in newborn mice and in the uterine epithelium on day 4 after birth [16,37].…”

“…Neonatal DES treatment should influence the ER system of both stromal and epithelial cells during the period of neonatal DES exposure even in the uterus, because a single DES injection increased ERa protein and mRNA levels within several hours in the uterine epithelial cells of newborn and 4-day-old mice [30,37]. In addition, perinatal DES treatment was reported to accelerate the onset of ERa synthesis in the uterine, cervical and vaginal epithelium of neonatal mice [11,31].…”